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Open AccessArticle

Sulfasalazine Attenuates Staphylococcal Enterotoxin B-Induced Immune Responses

Department of Immunology, Molecular Translational Sciences Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21702-5011, USA
Academic Editor: Yukako Fujinaga
Toxins 2015, 7(2), 553-559;
Received: 4 December 2014 / Accepted: 27 January 2015 / Published: 13 February 2015
(This article belongs to the Special Issue Enterotoxins: Microbial Proteins and Host Cell Dysregulation)
Staphylococcal enterotoxin B (SEB) and related exotoxins are important virulence factors produced by Staphylococcus aureus as they cause human diseases such as food poisoning and toxic shock. These toxins bind directly to cells of the immune system resulting in hyperactivation of both T lymphocytes and monocytes/macrophages. The excessive release of proinflammatory cytokines from these cells mediates the toxic effects of SEB. This study examined the inhibitory activities of an anti-inflammatory drug, sulfasalazine, on SEB-stimulated human peripheral blood mononuclear cells (PBMC). Sulfasalazine dose-dependently inhibited tumor necrosis factor α, interleukin 1 (IL-1) β, IL-2, IL-6, interferon γ (IFNγ), and various chemotactic cytokines from SEB-stimulated human PBMC. Sulfasalazine also potently blocked SEB-induced T cell proliferation and NFκB activation. These results suggest that sulfasalazine might be useful in mitigating the toxic effects of SEB by blocking SEB-induced host inflammatory cascade and signaling pathways. View Full-Text
Keywords: staphylococcal enterotoxin B; inflammatory cytokines; sulfasalazine staphylococcal enterotoxin B; inflammatory cytokines; sulfasalazine
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Krakauer, T. Sulfasalazine Attenuates Staphylococcal Enterotoxin B-Induced Immune Responses. Toxins 2015, 7, 553-559.

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